文献类型：期刊文献

英文题名：N-acetyl-L-cysteine attenuated the toxicity of ZIF-8 on EA.hy926 endothelial cells by wnt/beta-catenin pathway

作者：Tang, Yaxin[1];Jin, Lifang[1,5];Qi, Wenwen[2];Gao, Yue[1];Xie, Yixia[1];Xie, Xueying[1];Lv, Jianan[1];Jiang, Zhikai[3];Jiang, He[4];Fan, Caixia[1];Yan, Junyan[1]

机构：[1]Shaoxing Univ, Sch Life Sci, Shaoxing 312000, Zhejiang, Peoples R China;[2]Xiangzhou Dist Peoples Hosp, Xiangyang, Hubei, Peoples R China;[3]Wenzhou Med Univ, Clin Med Coll 2, Wenzhou, Zhejiang, Peoples R China;[4]Zhejiang Chinese Med Univ, Clin Med Sch 1, Hangzhou, Peoples R China;[5]Zhejiang Sci Tech Univ, Shaoxing Acad Biomed, Shaoxing, Zhejiang, Peoples R China

年份：2023

卷号：88

外文期刊名：TOXICOLOGY IN VITRO

收录：SCI-EXPANDED(收录号：WOS:000994024700001)、、Scopus(收录号：2-s2.0-85146129235)、WOS

基金：This work was supported by research grants from the Natural Science Foundation of Zhejiang Province (NO. LQ20B070003) , and Zhejiang Province Science and Technology Project of China (No. 2018C37105) . The project was also supported by Open Fund of Shaoxing Academy of Biomedicine of Zhejiang Sci-Tech University (SXAB202015) .

语种：英文

外文关键词：ZIF-8; EA; hy926 endothelial cells; N-acetyl-L-cysteine (NAC); Toxicity

外文摘要：As kinds of porous crystalline compounds, zeolitic imidazolate frameworks (ZIFs) have been developed quickly and attracted considerable attention for use in nano drug delivery systems, which raised concerns about cardiovascular disorders. At the present, the cytotoxic mechanism of ZIFs in cardiovascular disorders was still unclear. Our experiment explored the toxicity of ZIF-8, a typical kind of ZIFs, on human EA.hy926 vascular endothelial cells. The cell viability, ROS formation, apoptosis level, inflammatory response level, wound healing ability and atherosclerosis-related indicators of EA.hy926 endothelial cells were analyzed after ZIF-8 treatment. Meanwhile, we evaluated the ability of antioxidant N-Acetyl-L-cysteine (NAC) to attenuate the toxicity of ZIF-8 on EA.hy926 endothelial cells. As results, NAC attenuated ROS formation, cell apoptosis, LDH formation and endothelial dysfunction caused by ZIF-8. As the Wnt/beta-catenin pathway was involved in endothelial cell dysfunction, we also studied the expression level of beta-catenin and LEF1 in ZIF-8 and/or NAC treated EA.hy926 cells. As expected, ZIF-8 increased the protein expressions of beta-catenin and LEF1in the IC50 group, which was significantly inhibited by co-treatment with NAC. Taken together, this study could help improve our understanding about the mechanism of ZIF-8-induced endothelial cells injury and NAC had therapeutic potential in preventing ZIF-8-associated endothelial dysfunction by wnt/beta-catenin pathway.